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Mouse embryonic kidneys (E13.5): mutant (UB HDAC1,2-/-) vs. wild type

ABSTRACT: Transcriptional profiling of mouse embryonic kidneys (E13.5) comparing UB HDAC1,2-/- kidneys with wild type kidneys. Studies in our lab showed that histone deacetylase 1 (HDAC1) and 2 (HDAC2) perform redundant, yet essential functions in the developing mouse ureteric bud (UB) tissue. Double deletion of HDAC1 and HDAC2 in the UB results in impaired UB branching morphogenesis, followed by severe kidney dysgenesis. The goal of the microarray analysis was to identify the genetic pathways controlled by HDAC1 and 2 in the UB.

ORGANISM(S): Mus musculus

PROVIDER: GSE35432 | GEO | 2012/01/31

SECONDARY ACCESSION(S): PRJNA152771

REPOSITORIES: GEO

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Mouse embryonic kidneys (E13.5): mutant (UB HDAC1,2-/-) vs. wild type

Project description:Transcriptional profiling of mouse embryonic kidneys (E13.5) comparing UB HDAC1,2-/- kidneys with wild type kidneys. Studies in our lab showed that histone deacetylase 1 (HDAC1) and 2 (HDAC2) perform redundant, yet essential functions in the developing mouse ureteric bud (UB) tissue. Double deletion of HDAC1 and HDAC2 in the UB results in impaired UB branching morphogenesis, followed by severe kidney dysgenesis. The goal of the microarray analysis was to identify the genetic pathways controlled by HDAC1 and 2 in the UB. Two-condition experiment: E13.5 mutant kidneys (UB HDAC1,2-/-) vs. E13.5 wild type kidneys . Biological replicates: 4 control replicates, 4 UB HDAC1,2-/- replicates. Two-color Agilent 4x44k chips with dye-swaps on 2 of 4 arrays.

2012-01-31 | E-GEOD-35432 | biostudies-arrayexpress

Mouse embryonic kidneys (E13.5): HDAC inhibitor (HDACi) treated vs. Control

Project description:Transcriptional profiling of cultured CD1 mouse embryonic kidneys (E13.5) comparing HDACi-treated kidneys with control drug-treated kidneys. Studies in our lab showed that pharmacological inhibition of HDAC activity in ex-vivo cultured metanephroi results in extensive defects in kidney development, including impaired UB branching, tubulogenesis, and glomerulogenesis, accompanied by cell cycle arrest and apoptosis.The goal of the microarray analysis was to elucidate the morphogenetic pathways affected by HDACi. Two-condition experiment, HDACi-treated E13.5 kidneys (Scriptaid 2.0 μg/ml x 6hrs) vs. Control drug-treated E13.5 kidneys (Nullscript 2.0 μg/ml x 6hrs). Biological replicates: 3 control replicates, 3 HDACi-treated replicates. Two-color Agilent 4x44k chips with dye-swap on 2 of 4 arrays.

2010-08-01 | E-GEOD-19581 | biostudies-arrayexpress

Mouse embryonic kidneys (E13.5): HDAC inhibitor (HDACi) treated vs. Control

2010-08-01 | GSE19581 | GEO

miRNA expression data from embryonic ureteric bud (UB) cells

Project description:UB cells FACS sorted from E15.5 mouse kidneys were analyzed for miRNAs expression.

2014-08-28 | GSE60845 | GEO

Expression data from mouse embryonic ureteric bud (UB) cells

Project description:Dicer-dependent miRNAs are required for UB morphogenesis and differentiation during metanephric kidney development. We used microarray analysis to identify genes whose expression in the UB epithelium are altered from UB-specific ablation of Dicer. E15.5 UB cells from control and Dicer mutant kidneys were FACS sorted for transcription profiling.

2014-08-27 | E-GEOD-60758 | biostudies-arrayexpress

miRNA expression data from embryonic ureteric bud (UB) cells

Project description:UB cells FACS sorted from E15.5 mouse kidneys were analyzed for miRNAs expression. E15.5 UB cells FACS sorted from Rosa26YFP; Hoxb7Cre mice, total RNAs including miRNAs were purified and used for miRNA microarray

2014-08-28 | E-GEOD-60845 | biostudies-arrayexpress

Stabilization of ß-catenin during murine Kidney Development

Project description:We define a pathogenic role for a ß-catenin-activated genetic pathway in murine renal dysplasia. Cre-mediated stabilization of ß-catenin in the ureteric cell lineage prior to the onset of kidney development increased ß-catenin levels and caused renal aplasia or severe hypodysplasia. A genome-wide analysis of mRNA expression in dysplastic tissue identified down-regulation of genes required for ureteric branching and up regulation of Tgfß2 and Dkk1. Hoxb7-Cre:EGFP mice ( Zhao, et al. (2004) Dev Biol 276:403-415) were crossed with mice containing loxP sites flanking exon 3 of the ß-catenin allele (ß-catdelta3/delta3) (Harada,et al. (2002) Cancer Res 62:1971-1977) to generate ß-catenin gain-of-function mutant mice specific to the uteric bud, termed ß-catGOF-UB .Eighteen ß-catGOF-UB mutant kidneys and 9 WT kidneys were micro-dissected at E12.5. Mutant kidneys were divided into three random pools (n=3) consisting of 6 kidneys each and mRNA expression assessed by microarray.

2011-03-28 | E-GEOD-20325 | biostudies-arrayexpress

Whole kidneys at embryonic day 14.5: wildtype (WT) versus Hoxb7Cre transgene mediated conditional Mdm4 knockout kidneys

Project description:Transcriptional profiling of mouse embryonic kidneys lacking Mdm4 function in the ureteric bud lineage

2020-06-01 | GSE137994 | GEO

Transcripts identified by microarray analysis that were deregulated in E13.5 Tbx18cre/+;HprtTbx2/Y (Tbx2-GOF) ureters

Project description:Evaluation of the transcriptional changes in E13.5 ureters upon overexpression of Tbx2 in the ureteric mesenchyme.

2018-11-16 | GSE122558 | GEO

Proteomic profiling in mouse kidneys post-UUO

Project description:Increased export of transglutaminase-2 (TG2) by tubular epithelial cells (TECs) into the surrounding interstitium modifies the extracellular homeostatic balance leading to fibrotic membrane expansion. Although silencing of extracellular TG2 ameliorates progressive kidney scarring in animal models of chronic kidney disease, the pathway through which TG2 is secreted from TECs and contributes to disease progression has not been elucidated. In this study, we developed a global proteomic approach to identify binding partners of TG2 responsible for TG2 externalization in kidneys subjected to unilateral ureteric obstruction, using TG2-knockout kidneys as negative controls. We report a robust and unbiased analysis of the membrane interactome of TG2 in fibrotic kidneys relative to the entire proteome post-UUO detected by SWATH-mass spectrometry.

2018-02-07 | PXD008173 | Pride

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